Capillaries are of central importance in the three most common retinal vascular diseases in man: diabetic retinopathy (DR), hypertensive retinopathy (HR) and vein occlusion (VO). The cells forming the capillary wall, endothelial cells and pericytes, contain a structural apparatus which involves actin and fibronectin (FN) and suggests capillary contractile function. During DR, HR and VO the capillary contractile apparatus is subject to stress and may structurally change. Thus, our AIM I is to evaluate: 1. The content and distribution of actin in capillary pericytes and endothelial cells using the myosin subfragment-1 (S-1) technique for actin staining and quantitative morphometry. 2. The coexistence and coextensions of actin and FN (=fibronexus, FNX) in capillary pericytes localized and endothelial cells using mainly EM immunocytochemistry (immunoferritin). I,1. and I,2. are to be examined in 4 model situations: DR in rats and human, HR in rats, VO in monkeys. Preretinal membranes (PRM's) are part of proliferative vitreoretinopathy (PVR) an important cause of human blindness. PRM's are intraocular scar tissue that shrinks causing retinal detachment and atrophy. The scar tissue develops by proliferation and migration of a variety of cells whose identity is not fully known. Contraction of PRM's seems to be a cell-mediated event and may involve actin and FNX relationships. Thus, our AIM II is to evaluate: 1. The identity of proliferating and migrating cells during the development of PRM's using LM immunohistochemistry (immunoperoxidase) with markers for glial cells (GFAP), epithelial cells (prekeratin and keratin) and endothelial cells (Factor VIII-related antigen). 2. The presence of FNX relationships by both LM and EM immunocytochemistry. II,1. and II,2. are to be examined in 3 model situations: PRM's produced by injection of colloidal carbon into the vitreous of rabbits and monkeys, and spontaneous PRM's developing during human PVR.